Evidence map›Paper›PMID 25532528›Full record

ArticleCirculation. Arrhythmia and electrophysiology2015

Sympathetic nerve stimulation, not circulating norepinephrine, modulates T-peak to T-end interval by increasing global dispersion of repolarization.

Daigo Yagishita, Ray W Chui, Kentaro Yamakawa, Pradeep S Rajendran, Olujimi A Ajijola, Keijiro Nakamura, Eileen L So, Aman Mahajan, Kalyanam Shivkumar, Marmar Vaseghi

Open access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation. Arrhythmia and electrophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
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  13. Stellate ganglia stimulation counteracts vagal stimulation by significantly increasing heart rate and blood pressure.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2025
    Article
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  16. Management of patients with an electrical storm or clustered ventricular arrhythmias: a clinical consensus statement of the European Heart Rhythm Association of the ESC-endorsed by the Asia-Pacific Heart Rhythm Society, Heart Rhythm Society, and Latin-American Heart Rhythm Society.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024
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  20. Status of βReviews in cardiovascular medicine · 2023
    Review

12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Daigo YagishitaFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles.
Ray W ChuiFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles.
Kentaro YamakawaFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles.
Pradeep S RajendranFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles.
Olujimi A AjijolaFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles.
Keijiro NakamuraFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles.
Eileen L SoFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles.
Aman MahajanFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles.
Kalyanam ShivkumarFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles.
Marmar VaseghiFrom the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles. mvaseghi@mednet.ucla.edu.
Norwegian Womens Public Health Association · NO

Funding

ELECTROPHYSIOLOGICAL EFFECTS OF NEURAL REMODELING OF THE VENTRICLESR01HL084261 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHIVKUMAR, KALYANAM · 2006 to 2016
$3.4M
Training in Molecular, Cellular &Integrative PhysiologyT32GM065823 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2003 to 2017
$2.1M
Antiarrhythmic Mechanisms of Bilateral Cardiac Sympathetic DecentralizationK08HL125730 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A · 2015 to 2019
$833k
NHLBI NIH HHS K08 HL125730NHLBI NIH HHS R01 HL084261NHLBI NIH HHS R01HL084261NIGMS NIH HHS T32 GM065823
6 · The paper itself

Abstract

backgroundT-peak to T-end interval (Tp-e) is an independent marker of sudden cardiac death. Modulation of Tp-e by sympathetic nerve activation and circulating norepinephrine is not well understood. The purpose of this study was to characterize endocardial and epicardial dispersion of repolarization (DOR) and its effects on Tp-e with sympathetic activation. METHODS AND

resultsIn Yorkshire pigs (n=13), a sternotomy was performed and the heart and bilateral stellate ganglia were exposed. A 56-electrode sock and 64-electrode basket catheter were placed around the epicardium and in the left ventricle (LV), respectively. Activation recovery interval, DOR, defined as variance in repolarization time, and Tp-e were assessed before and after left, right, and bilateral stellate ganglia stimulation and norepinephrine infusion. LV endocardial and epicardial activation recovery intervals significantly decreased, and LV endocardial and epicardial DOR increased during sympathetic nerve stimulation. There were no LV epicardial versus endocardial differences in activation recovery interval during sympathetic stimulation, and regional endocardial activation recovery interval patterns were similar to the epicardium. Tp-e prolonged during left (from 40.4±2.2 ms to 92.4±12.4 ms; P<0.01), right (from 47.7±2.6 ms to 80.7±11.5 ms; P<0.01), and bilateral (from 47.5±2.8 ms to 78.1±9.8 ms; P<0.01) stellate stimulation and strongly correlated with whole heart DOR during stimulation (P<0.001, R=0.86). Of note, norepinephrine infusion did not increase DOR or Tp-e.

conclusionsRegional patterns of LV endocardial sympathetic innervation are similar to that of LV epicardium. Tp-e correlated with whole heart DOR during sympathetic nerve activation. Circulating norepinephrine did not affect DOR or Tp-e.

Indexed as

Action PotentialsAdrenergic alpha-AgonistsAnimalsDeath, Sudden, CardiacDisease Models, AnimalElectric StimulationEndocardiumFemaleHeart VentriclesHemodynamicsInfusions, IntravenousNorepinephrinePericardiumStellate GanglionTime FactorsAdrenergic alpha-AgonistsNorepinephrineaction potentialautonomic nervous systemdispersionECGsympatheticT wave

Identifiers

PMID25532528
PMCPMC4405126
OpenAlexW2127160628

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.